Natural pharmaceuticals play an important role in the research of the field of medical care and pharmaceutical research. It is shown that 80% of antimicrobial drugs and 60% anticancer drugs originate directly or indirectly from natural products (J Nat Prod, 2003, 66: 1022-1237).
Resina Toxicodendri is the dried resin secreted by Toxicodendron vernicifluum and has been used as an anti-inflammatory and anti-scarring agent in traditional Chinese medicine for centuries.
Chinese patent application no. 201010149042.3, titled “Urushiol compound and medicinal composition thereof, preparation method and application” thereof, filed on Apr. 16, 2010, published on Aug. 18, 2010 with publication no. CN101805246A, granted on Jun. 5, 2013, disclosed that the researchers of Kunming Institute of Botany, Chinese Academy of Sciences (Kunming, China) isolated and purified an urushiol compound with the following structural formula:

The above urushiol compound is marked with a code GQ-5. GQ-5 is a small molecular urushiol compound with a molecular formula, C21H34O2. The compound preparation formed by the urushiol compound has obvious effects of inhibiting tumor cytotoxin activity and tumor angiogenesis.
Inventors of the present invention, from Southern Medical University (Guangzhou, China) continue the research of the phenolic component GQ-5 has effective of inhibiting fibrosis of liver tissue and kidney tissue. They filed the following two Chinese patent applications: CN 201010149042.3, titled “Use of an urushiol compound in preparation of drug for inhibiting fibrosis of liver tissue”, filed on Apr. 17, 2012, published on Oct. 30, 2013 with publication no. CN103371986A; CN 201210111642.X, titled “Use of an urushiol compound in preparation of drug for inhibiting fibrosis of kidney tissue”, filed on Apr. 17, 2012, published on Oct. 30, 2013 with publication no. CN103371987A.
All patents, patent publications, and non-patent publications cited are incorporated by reference herein.
TGF-β1 signals are transduced by transmembrane serinethreonine kinase receptors type I (TβRI) and type II (TβRII) and intracellular mediators known as Smads. Upon TGF-β1 stimulation, Smad2 and Smad3 are phosphorylated by TβRI. Phosphorylated Smadsheteroligomerize with the common partner Smad4 and then translocate into the nucleus, where they control the transcription of TGF-β-responsive genes through interaction with specific cis-acting elements in the regulatory regions. Although both Smad2 and Smad3 are strongly activated in various experimental and human fibrotic kidney diseases, it is now well recognized that Smad3 is the key mediator of TGF-β1-induced ECM production and tissue fibrosis. Deletion of Smad3 suppresses fibrogenesis in a number of rodent models, including diabetic nephropathy, obstructive nephropathy, and drug toxicity-related nephropathy. On the other hand, conditional knocking out of Smad2 from kidney tubular cells significantly enhanced renal fibrosis via up-regulation of Smad3 signaling. These findings indicate that Smad3 expression and/or phosphorylation might be a potential target for the intervention of renal fibrosis.